An interquartile increase of only 3 µg/m3 in
exposure to particulate matter less than 2.5 µg in diameter was associated with
a decrease of 0.3 percent in flow-mediated dilation of the brachial artery,
according to Ranjini M. Krishnan, MD, of the University of Washington in
Seattle, and colleagues.

The magnitude of that percentage increase of flow-mediated dilation
"is comparable to the effect of 5 years' increase in age, or of active
tobacco smoking," the researchers explained online in the Journal
of the American College of Cardiology.

Epidemiologic studies have identified an association between air
pollution and cardiovascular disease, and experiments have suggested that
exposure to air pollution can lead to endothelial dysfunction.

To explore the hypothesis that exposure to particulate matter can lead
to persistent endothelial compromise and the attendant effects on the
vasculature, Krishnan and colleagues analyzed data from the Multi-Ethnic Study
of Atherosclerosis and Air Pollution (MESA).

The cohort included 3,040 participants living in Chicago, Los Angeles,
New York, St. Paul, and Winston-Salem, N.C.

Median age was 61, and the sexes were equally represented. One-third
of the participants were white, while the remainder were African-American,
Chinese, or Hispanic.

Slightly more than half had never smoked, and 34 percent were taking
antihypertensive medications.

A statistically significant −0.1 percent difference was seen in
flow-mediated dilation according to long-term concentration of fine particulate
matter, the researchers found.

In contrast, only nonsignificant reductions in flow-mediated dilation
were seen for short-term exposures.

This observation of minimal effects with short-term exposure was
similar to what has been seen in previous cohort studies, where a 1-day 10
µg/m3 increase in exposure was associated with a
mortality increase of only 0.1 percent to 0.5 percent, compared with a 10
percent increase seen with long-term exposure.

The association between change in flow-mediated dilation and
particulate matter exposure was consistent across the study locations, with the
exception of St. Paul, which had lower concentrations of pollutants than the
other cities.

The strongest association was seen in Chicago.

Further analysis revealed a large effect for younger age, with a
reduction of −0.5 percent in brachial artery dilation.

Greater effects also were seen for women, nonsmokers, and individuals
with mild hypertension.

One factor that appeared to ameliorate the influence of particulate
matter on endothelial function was the use of angiotensin-converting enzyme
inhibitors, possibly through effects on endothelial kinins and nitric oxide,
the researchers explained.

Proposed mechanisms by which pollutants could induce changes in blood
vessels include inflammation, oxidative stress, and effects on the autonomic
nervous system.

In an editorial comment, Robert D. Brook, MD, of the University of
Michigan in Ann Arbor, and Sanjay Rajagopalan, MD, of Ohio State University in
Columbus, noted that an implication of the study was that even modest increases
in air pollution levels can have significant and "clinically
pertinent" negative effects on vascular function.

"This novel observation should re-awaken us to the fact that even
'invisible' elements, such as chronic exposure to low levels of air pollution
commonly encountered in the United States, can have significant adverse effects
on [cardiovascular] health," stated Brook and Rajagopalan.

And the health hazards may be worse elsewhere, they
suggested.

"When one considers the fact that [fine particulate matter]
levels often average 5- to 10-fold higher across numerous regions populated by
billions of people worldwide, the grave global public health consequences of
air pollution corroborated by the findings of this important study deserve
serious and immediate attention," the editorialists concluded.

Limitations of the study included its cross-sectional design and the
possibility of measurement errors with the modeling methods used.

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